Overdrive Pacing in Quinidine Syncope and Other Long QT-Interval Syndromes

DiSegni, Elio; Klein, Herman O.; David, Daniel; Libhaber, Carlos D.; Kaplinsky, Elieser

doi:10.1001/archinte.1980.00330190048018

Cited by 57 publications

(7 citation statements)

References 21 publications

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“…The probability of maintaining sinus rhythm cardia. [28] (in those that converted) for 1 year was 79% with dofetilide versus Although class III antiarrhythmic drugs are widely considered 42% in the control group (p < 0.001). Even though dofetilide had to be effective for prophylaxis against frequent shocks, there are no effect on all-cause mortality, presence of sinus rhythm in either surprisingly few controlled studies that demonstrate this (table treatment group was associated with a significant reduction in II).…”

mentioning

confidence: 97%

Antiarrhythmic Drugs in Patients with Implantable Cardioverter-Defibrillators

Bollmann

Husser

Cannom

2005

American Journal of Cardiovascular Drugs

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Antiarrhythmic drugs need to be initiated in up to 70% of patients with implantable cardioverter-defibrillators (ICDs) in order to treat atrial tachyarrhythmias, decrease the frequency of defibrillator shocks, and terminate ventricular arrhythmias along with antitachycardia pacing. trial fibrillation (AF) occurs in about 20% of patients with ICDs (the majority with congestive heart failure [CHF]). Antiarrhythmic drugs are initiated for this indication in 2-20% of the ICD population. Data from CHF-STAT (Congestive Heart Failure: Survival Trial of Antiarrhythmic Therapy; amiodarone vs placebo) and DIAMOND-AF (Danish Investigations of Arrhythmia and Mortality ON Dofetilide--rial Fibrillation; dofetilide vs placebo) support the approach that restoration and maintenance of sinus rhythm might be beneficial in CHF, even though no study has specifically addressed the CHF population with ICDs. Further clarification on potential benefits of rhythm control in CHF-associated AF will come from the AF-CHF (Atrial Fibrillation and Congestive Heart Failure) trial that is currently underway. The vast majority of patients with ICDs will have discharges of their devices during follow-up. Although class III antiarrhythmic drugs are widely considered to be effective for prophylaxis against frequent shocks, there are surprisingly few controlled studies that demonstrate this. In contrast to conflicting amiodarone data, sotalol has been found to be effective in preventing shocks from ICDs in prospective, randomized, placebo-controlled studies. A large study (SHIELD; SHock Inhibition Evaluation with azimiLiDe) has shown that azimilide significantly reduces ventricular tachyarrhythmia recurrence, thereby reducing the burden of symptomatic ventricular tachyarrhythmia. Other novel antiarrhythmic drugs, such as dofetilide or dronedarone, as well as different strategies (e.g. in the OPTIC [Optimal Pharmacological Therapy in Implantable Cardioverter] trial; beta-adrenoceptor antagonist therapy alone, amiodarone plus beta-adrenoceptor antagonist therapy, or sotalol alone) for the prevention of ICD shocks are under evaluation. The majority of antiarrhythmic drugs, including sotalol, dofetilide, and azimilide, have no effect on, or are even associated with a decrease in, defibrillation thresholds in humans. Amiodarone, in contrast, has been shown to be related to higher defibrillation thresholds at implant and during follow-up of monophasic devices. Potential cardiac (e.g. ventricular proarrhythmia, negative inotropic effect) and drug-specific non-cardiac adverse effects are a frequent cause for drug discontinuation and need to be considered when initiating and maintaining antiarrhythmic drug therapy. In conclusion, antiarrhythmic drugs are frequently used in ICD patients, the main indications being treatment of atrial tachyarrhythmias and prevention of ICD shocks. Despite potential adverse effects, antiarrhythmics can be administered safely, as long as ICD/drug interactions are appreciated. Controlled studies that will further define the role of...

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confidence: 97%

Antiarrhythmic Drugs in Patients with Implantable Cardioverter-Defibrillators

Bollmann

Husser

Cannom

2005

American Journal of Cardiovascular Drugs

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“…Temporary ventricular overdrive pacing can also be used in the short term [12, 13]. It prevents bradycardias and pauses and decreases the QT interval due an increase in heart rate.…”

Section: Discussionmentioning

confidence: 99%

Torsades de pointes and self‐terminating ventricular fibrillation in a prescription methadone user

2007

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SummaryMethadone is known to prolong the QT interval and precipitate torsades de pointes. A 54-year-old prescription methadone user with hypokalaemia was referred to Critical Care with acute confusion and respiratory distress. Alcohol withdrawal was the presumed precipitant. The real precipitant only became evident on analysis of a 24-h ECG (Holter monitor) attached to the patient at the time. The patient had suffered prolonged (10 min) ventricular arrhythmias including torsades de pointes and self-terminating ventricular fibrillation. The patient made a full recovery. Risk factors for acquired long QT syndrome and the treatment of torsades de pointes are discussed. Methadone is a synthetic opioid used in the treatment of severe pain and opioid addiction. In 2005, there were over 88 000 prescriptions for methadone dispensed in the community in England [1]. It is also a drug of abuse with approximately 11 000 16-59-year-olds in England and Wales using it in the year 2004 ⁄ 5 [2]. In 2002, a case series first established the association between methadone and acquired long QT syndrome with its potentially lifethreatening sequelae torsades de pointes [3]. This association is now well established. Case reportA 54-year-old man presented to the emergency department with epigastric pain and vomiting. No cardiovascular symptoms were described. Past medical history included chronic pancreatitis, alcoholism, hypertension and intravenous drug use until 2 years previously. He was taking methadone 60 mg orally per day. Examination demonstrated epigastric tenderness but no cardiovascular or other abnormality. Serum potassium was 2.6 mmol.l Other routine blood tests including amylase and magnesium were normal.ECG showed sinus rhythm, prolonged QT interval (QTc ¼ 0.64 s), peaked P waves and biphasic T waves (Fig. 1). No previous ECG was available for comparison. A diagnosis of pain related to chronic pancreatitis and vomiting-induced hypokalaemia was made. He was placed nil by mouth, given intramuscular morphine for analgesia, anti-emetics and intravenous fluids with potassium supplementation. Methadone was continued intravenously.An echocardiogram and 24-h ambulatory ECG (Holter monitor) were organised in view of the abnormal ECG and a computed tomography (CT) of the abdomen requested. The patient's symptoms settled within 48 h. Echocardiogram demonstrated mild left ventricular hypertrophy with normal function. CT abdomen showed only an atrophic pancreas. Sixty hours after admission (around 04.00 h), the patient became acutely confused on the medical ward. The 24-h ECG was in progress at this time. Following review by the medical team, a diagnosis of alcohol withdrawal was made and intravenous lorazepam administered. Over the following 6 h the patients remained agitated and confused, requiring further doses of lorazepam. He became increasingly tachypnoeic and hypoxic and a referral to Critical Care was made.On arrival the patient's observations were as follows: saturation 77% on 15 l face mask oxygen, respiratory rate 40 breath...

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“…Temporary Transvenous Cardiac Pacing -If electrolyte replacement does not prevent PVT a temporary transvenous pacing wire should be inserted and set to pace at 90-110 beats per minute [51].…”

Section: A Practical Framework For Preventing Qtc Prolongation and Itmentioning

confidence: 99%

Prolongation of the Corrected QT Complex – A Cause of Sudden Cardiac Death in the Mountain Environment?

et al. 2011

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In the mountain environment sudden cardiac death (SCD) has been shown to be responsible for the deaths of up to 52% of downhill skiers and 30% of hikers. The majority of SCD's are precipitated by a ventricular arrhythmia. Although most are likely to result from structural abnormalities associated with conditions such as ischaemic heart disease, a small but significant number may be due to abnormalities in ion channel activity, commonly known as, "channelopathies". Channelopathies have the potential to lengthen the time between ventricular depolarisation and repolarisation that can result in prolongation of the corrected QT interval (QTc) and episodes of polymorphic ventricular tachycardia (PVT) and eventually, ventricular fibrillation. This review examines the factors that prolong the QTc interval in the mountain environment and outlines a practical framework for preventing the life threatening arrhythmias that are associated with this condition.

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Overdrive Pacing in Quinidine Syncope and Other Long QT-Interval Syndromes

Cited by 57 publications

References 21 publications

Antiarrhythmic Drugs in Patients with Implantable Cardioverter-Defibrillators

Antiarrhythmic Drugs in Patients with Implantable Cardioverter-Defibrillators

Torsades de pointes and self‐terminating ventricular fibrillation in a prescription methadone user

Prolongation of the Corrected QT Complex – A Cause of Sudden Cardiac Death in the Mountain Environment?

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